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1. Toll-like receptor 3 activation is required for normal skin barrier repair following UV damage.

Author

Borkowski, Andrew W, Kuo, I-Hsin, Bernard, Jamie J, Yoshida, Takeshi, Williams, Michael R, Hung, Nai-Jung, Yu, Benjamin D, Beck, Lisa A, and Gallo, Richard L

Subjects
Tight Junctions, Keratinocytes, Skin, Animals, Mice, Inbred C57BL, Mice, Poly I-C, Cytokines, Ultraviolet Rays, Permeability, Female, Male, Toll-Like Receptor 3, Inbred C57BL, Clinical Sciences, Oncology and Carcinogenesis, Dermatology & Venereal Diseases
Abstract

UV damage to the skin leads to the release of noncoding RNA (ncRNA) from necrotic keratinocytes that activates Toll-like receptor 3 (TLR3). This release of ncRNA triggers inflammation in the skin following UV damage. Recently, TLR3 activation was also shown to aid wound repair and increase the expression of genes associated with permeability barrier repair. Here, we sought to test whether skin barrier repair after UVB damage is dependent on the activation of TLR3. We observed that multiple ncRNAs induced expression of skin barrier repair genes, that the TLR3 ligand Poly (I:C) also induced expression and function of tight junctions, and that the ncRNA U1 acts in a TLR3-dependent manner to induce expression of skin barrier repair genes. These observations were shown to have functional relevance as Tlr3-/- mice displayed a delay in skin barrier repair following UVB damage. Combined, these data further validate the conclusion that recognition of endogenous RNA by TLR3 is an important step in the program of skin barrier repair.

Published
2015

4. Phenome‐Wide Association Study of Autoantibodies to Citrullinated and Noncitrullinated Epitopes in Rheumatoid Arthritis

Author

Liao, Katherine P., primary, Sparks, Jeffrey A., additional, Hejblum, Boris P., additional, Kuo, I‐Hsin, additional, Cui, Jing, additional, Lahey, Lauren J., additional, Cagan, Andrew, additional, Gainer, Vivian S., additional, Liu, Weidong, additional, Cai, T. Tony, additional, Sokolove, Jeremy, additional, and Cai, Tianxi, additional

Published
2017
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6. Abstracts from the 15th International Myopia Conference

Author

Benavente-Perez, Alexandra, primary, Nour, Ann, additional, Ansel, Tobin, additional, Abarr, Kathleen, additional, Yan, Luying, additional, Roden, Keisha, additional, Troilo, David, additional, Lu, Chanyi, additional, Pan, Miaozhen, additional, Zheng, Min, additional, Qu, Jia, additional, Zhou, Xiangtian, additional, Wildsoet, Christine F., additional, Lu, Fan, additional, Chen, Jie, additional, Bao, Jinhua, additional, Hu, Liang, additional, Wang, Qinmei, additional, Jin, Zibing, additional, Rucker, Frances, additional, Britton, Stephanie, additional, Hanowsky, Stephan, additional, Spatcher, Molly, additional, Kuo, Hui-Ying, additional, Ke, Ching-Hsiu, additional, Kuo, I-Hsin, additional, Peng, Chien-Chun, additional, Sun, Han-Yin, additional, Morgan, Ian G., additional, Guggenheim, Jeremy A., additional, Shah, Rupal L., additional, Williams, Cathy, additional, Yang, Jinglei, additional, Reinach, Peter S., additional, Zhang, Sen, additional, Sun, Wenfeng, additional, Liu, Bo, additional, Li, Fen, additional, Li, Xiaoqing, additional, Zhao, Aihua, additional, Chen, Tianlu, additional, Jia, Wei, additional, Jiang, Jun, additional, Wu, Haoran, additional, Tsubota, Kazuo, additional, Ozawa, Hiroko, additional, Torii, Hidemasa, additional, Takamizawa, Shigemasa, additional, Kurihara, Toshihide, additional, Negishi, Kazuno, additional, Graef, Klaus, additional, Rathbun, Daniel, additional, Schaeffel, Frank, additional, Ghodsi, Ladan, additional, Stell, William K., additional, Pardue, Machelle T., additional, Chakraborty, Ranjay, additional, Park, Han na, additional, Sidhu, Curran S., additional, Iuvone, P. Michael, additional, Collins, Michael J, additional, Srinvasalu, Nethrajeith, additional, McFadden, Sally A., additional, Baird, Paul N., additional, Artal, Pablo, additional, Cho, Pauline, additional, Cheung, SW, additional, Wu, Pei-Chang, additional, Hoang, Quan V., additional, Lee, Duk C., additional, Landis, Erica G., additional, Bergen, Michael A., additional, Sidhu, Curran, additional, Hattar, Samer, additional, Stone, Richard A., additional, Metlapally, Ravi, additional, Li, Ruiqin, additional, Xu, Qinglin, additional, Zhong, Hong, additional, Pan, Chenglin, additional, Lan, Weizhong, additional, Li, Xiaoning, additional, Chen, Ling, additional, Yang, Zhikuan, additional, Read, Scott A., additional, Saw, Seang-Mei, additional, Weng, Shi-Jun, additional, Wu, Xiao-Hua, additional, Qian, Kang-Wei, additional, Li, Yun-Yun, additional, Xu, Guo-Zhong, additional, Huang, Furong, additional, Yang, Xiong-Li, additional, Zhong, Yong-Mei, additional, Smith, Earl L, additional, Arumugam, Baskar, additional, Hung, Li-Fang, additional, Ostrin, Lisa A., additional, Trier, Klaus, additional, Jong, Monica, additional, Holden, Brien A., additional, Lam, Thomas Chuen, additional, Shan, Samantha, additional, Zuo, Bing, additional, Tse, Dennis Yan-yin, additional, Bian, Jingfang, additional, Li, King-Kit, additional, Liu, Quan, additional, To, Chi-ho, additional, Gawne, Timothy J., additional, Siegwart, John T., additional, Ward, Alexander H., additional, Norton, Thomas T., additional, Zhang, Yan, additional, Liu, Yue, additional, Ho, Carol, additional, Phan, Eileen, additional, Hang, Abraham, additional, Eng, Emily, additional, and Wildsoet, Christine, additional

Published
2016
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7. Activation of Epidermal Toll-like Receptor 2 Enhances Tight Junction Function:Implications for Atopic Dermatitis and Skin Barrier Repair.

Author

Kuo, I-Hsin, Beck, Lisa A., Kuo, I-Hsin, and Beck, Lisa A.

Abstract

Thesis (Ph.D.)--University of Rochester. School of Medicine & Dentistry. Dept. of Pathology and Laboratory Medicine, 2013., Atopic dermatitis (AD) is a Th2-skewed, allergen-driven skin disease characterized by epidermal tight junction (TJ) defects and a propensity for Staphylococcus aureus (S. aureus) skin infections. One widely held hypothesis is that the leaky epithelial barrier promotes immunologic responsiveness to allergens through the skin. Toll-like receptor (TLR) 2, a key innate receptor responsive to S. aureus, was originally recognized for its antimicrobial actions, but recently it has been shown to regulate intestinal epithelial barrier. We hypothesized that an effective cutaneous innate immune response might also include skin barrier repair. Furthermore, this barrier repair response may be impaired in AD patients. To determine the importance of TLR2 in epidermal barrier function, we used primary human keratinocytes (PHK), discarded human skins and Tlr2-/- mice. The TLR2 agonist increased TJ protein expression and function in PHK and enhanced TJ barrier repair in a murine wound model that mimics the itch-scratch cycle observed in AD patients. Since AD is a Th2-polarized inflammatory disorder, we hypothesized that Th2 cytokines might impair this TLR2-mediated barrier repair function. Th2 cytokines decreased TLR2 protein expression and attenuated TLR2’s barrier repair function in PHK and human epidermis. STAT6VT mice with a hyper-Th2 immune profile had reduced epidermal TLR2 protein expression and impaired TJ barrier recovery in response to TLR2 agonist. Bringing this observation back to human AD, we observed that epidermal TLR2 protein immunoreactivity was significantly reduced in nonlesional and lesional AD skin as compared to nonatopic controls (NA). The intensity of the TLR2 staining inversely correlated with skin barrier integrity and two Th2 biomarkers (serum total IgE levels and circulating eosinophil counts). In summary, TLR2 activation enhances TJ barrier in murine and human epidermis and is an important part of an epidermal wound repair response. Th2 cytokines commonly

Published
2015

12. Activation of Epidermal Toll-Like Receptor 2 Enhances Tight Junction Function: Implications for Atopic Dermatitis and Skin Barrier Repair

Author

Kuo, I-Hsin, primary, Carpenter-Mendini, Amanda, additional, Yoshida, Takeshi, additional, McGirt, Laura Y., additional, Ivanov, Andrei I., additional, Barnes, Kathleen C., additional, Gallo, Richard L., additional, Borkowski, Andrew W., additional, Yamasaki, Kenshi, additional, Leung, Donald Y., additional, Georas, Steve N., additional, De Benedetto, Anna, additional, and Beck, Lisa A., additional

Published
2013
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13. Biomarkers of Disease Severity and Th2 Polarity Are Predictors of Atopic Dermatitis Subjects Who Are Colonized with S. Aureus

Author

Beck, Lisa A., primary, Yoshida, Takeshi, additional, De Benedetto, Anna, additional, Rhee, Seungshin, additional, Kuo, I-Hsin, additional, Reese, Jamie, additional, David, Gloria, additional, Schneider, Lynda C., additional, Paller, Amy, additional, Hanifin, Jon M., additional, Boguniewicz, Mark, additional, Barnes, Kathleen C., additional, and Leung, Donald Y.M., additional

Published
2013
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15. Effects of colchicine on risk of cardiovascular events and mortality among patients with gout: a cohort study using electronic medical records linked with Medicare claims.

Author

Solomon, Daniel H., Chih-Chin Liu, I-Hsin Kuo, Zak, Agnes, Kim, Seoyoung C., Liu, Chih-Chin, and Kuo, I-Hsin

Subjects
CARDIOVASCULAR disease related mortality, CARDIOVASCULAR diseases, COLCHICINE, CAUSES of death, GOUT, LONGITUDINAL method, MEDICAL record linkage, MEDICARE, RESEARCH funding, GOUT suppressants, RETROSPECTIVE studies
Abstract

Background: Colchicine may have beneficial effects on cardiovascular (CV) disease, but there are sparse data on its CV effect among patients with gout. We examined the potential association between colchicine and CV risk and all-cause mortality in gout.Methods: The analyses used data from an electronic medical record (EMR) database linked with Medicare claims (2006-2011). To be eligible for the study cohort, subjects must have had a diagnosis of gout in the EMR and Medicare claims. New users of colchicine were identified and followed up from the first colchicine dispensing date. Non-users had no evidence of colchicine prescriptions during the study period and were matched to users on the start of follow-up, age and gender. Both groups were followed for the primary outcome, a composite of myocardial infarction, stroke or transient ischaemic attack. We calculated HRs in Cox regression, adjusting for potential confounders.Results: We matched 501 users with an equal number of non-users with a median follow-up of 16.5 months. During follow-up, 28 primary CV events were observed among users and 82 among non-users. Incidence rates per 1000 person-years were 35.6 for users and 81.8 for non-users. After full adjustment, colchicine use was associated with a 49% lower risk (HR 0.51, 95% CI 0.30 to 0.88) in the primary CV outcome as well as a 73% reduction in all-cause mortality (HR 0.55, 95% CI 0.35 to 0.85, p=0.007).Conclusions: Colchicine use was associated with a reduced risk of a CV event among patients with gout. [ABSTRACT FROM AUTHOR]

Published
2016
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17. Cysteine-Rich 61 (CCN1) Enhances Chemotactic Migration, Transendothelial Cell Migration, and Intravasation by Concomitantly Up-Regulating Chemokine Receptor 1 and 2

Author

Lin, Been-Ren, primary, Chang, Cheng-Chi, additional, Chen, Li-Ro, additional, Wu, Ming-Hsun, additional, Wang, Ming-Yang, additional, Kuo, I-Hsin, additional, Chu, Chia-Yu, additional, Chang, King-Jen, additional, Lee, Po-Huang, additional, Chen, Wei-Jao, additional, Kuo, Min-Liang, additional, and Lin, Ming-Tsan, additional

Published
2007
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18. Phenome‐Wide Association Study of Autoantibodies to Citrullinated and Noncitrullinated Epitopes in Rheumatoid Arthritis

Author

Liao, Katherine P., Sparks, Jeffrey A., Hejblum, Boris P., Kuo, I‐Hsin, Cui, Jing, Lahey, Lauren J., Cagan, Andrew, Gainer, Vivian S., Liu, Weidong, Cai, T. Tony, Sokolove, Jeremy, and Cai, Tianxi

Subjects
Rheumatoid Arthritis
Abstract

Objective: Patients with rheumatoid arthritis (RA) develop autoantibodies against a spectrum of antigens, but the clinical significance of these autoantibodies is unclear. Using a phenome‐wide association study (PheWAS) approach, we examined the association between autoantibodies and clinical subphenotypes of RA. Methods: This study was conducted in a cohort of RA patients identified from the electronic medical records (EMRs) of 2 tertiary care centers. Using a published multiplex bead assay, we measured 36 autoantibodies targeting epitopes implicated in RA. We extracted all International Classification of Diseases, Ninth Revision (ICD‐9) codes for each subject and grouped them into disease categories (PheWAS codes), using a published method. We tested for the association of each autoantibody (grouped by the targeted protein) with PheWAS codes. To determine significant associations (at a false discovery rate [FDR] of ≤0.1), we reviewed the medical records of 50 patients with each PheWAS code to determine positive predictive values (PPVs). Results: We studied 1,006 RA patients; the mean ± SD age of the patients was 61.0 ± 12.9 years, and 79.0% were female. A total of 3,568 unique ICD‐9 codes were grouped into 625 PheWAS codes; the 206 PheWAS codes with a prevalence of ≥3% were studied. Using the PheWAS method, we identified 24 significant associations of autoantibodies to epitopes at an FDR of ≤0.1. The associations that were strongest and had the highest PPV for the PheWAS code were autoantibodies against fibronectin and obesity (P = 6.1 × 10−4, PPV 100%), and that between fibrinogen and pneumonopathy (P = 2.7 × 10−4, PPV 96%). Pneumonopathy codes included diagnoses for cryptogenic organizing pneumonia and obliterative bronchiolitis. Conclusion: We demonstrated application of a bioinformatics method, the PheWAS, to screen for the clinical significance of RA‐related autoantibodies. Using the PheWAS approach, we identified potentially significant links between variations in the levels of autoantibodies and comorbidities of interest in RA.

Published
2017
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